In AML, mutations in kinases such as FMS-like tyrosine kinase 3 (FLT3) can activate STAT5 independently of JAK2, particularly in the presence of co-occurring nucleophosmin (NPM1) or DNA methyltransferase 3A (DNMT3A) mutations, which further upregulate MYC and BCL2 (202–204). Here, STAT5B is linked to acute myeloid leukemia.